I’m just getting back to my desk after a several days in Puerto Vallarta, Mexico.

I had a little R & R, played some golf, and just enjoyed myself in general.  Had all the same kinds of food I wrote about in a post last year, so I returned well fed.  Now I’m tanned, fed, fit and ready to type, so it’s back to the grindstone.

Thanks to the poor economy, this trip was a little more exciting than previous trips.  At least the golf part.  When we pulled the carts up to the first green on the first day we played, the caddy told us to pull off the cart path and park the carts down by the green.  When we asked why, he replied, “Banditos.”

Turns out that hard times have driven many desperate people to turn to crime to feed their families.  According to the caddy, ‘banditos’ hide in the jungle along side the cart paths and come out while the players are on the green and steal anything they can get their hands on.  A few weeks before we got there, there was an actual armed robbery on the course.  Fortunately, our trip was without incident, so I returned home with all my belongings.  Didn’t even lose anything to the airlines, which is probably a more likely way to lose valuables than to banditos on the golf course.

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A study appeared this week sure to drive members of the low-fat and vegan tribes sprinting for their Protexid.

Ron Krauss and his group published a paper in the Articles in Press section of the American Journal of Clinical Nutrition (AJCN) stating there is no evidence that saturated fat intake increases the risk for heart disease.  The paper, titled Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease, is not a study per se, but is a meta-analysis, a compilation of numerous studies looking at the relationship between saturated fat intake and the risk for developing heart disease.

As I’ve discussed before on these pages, meta-analyses are not my favorite types of studies.  I’ve attacked them when they’ve been used to ‘prove’ the low-fat diets are better, so I can’t very well embrace meta-analyses when they present a conclusion I agree with.  And I really can’t embrace meta-analyses when they are compilations of observational studies, which are themselves next to worthless.

For those who don’t know, meta-analyses are compilation studies in which researchers comb the medical literature for papers on a particular subject and then combine all the data  from the individual studies together into one large study.  This combining is often done to bring together a collection of studies, none of which contain data that has reached statistical significance, to see if the aggregate of all the data in the studies reaches statistical significance.  I think these types of meta-analyses are highly suspect, because they can lead to conclusions not warranted by the actual data.

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Synchronicity strikes again.  The seeds of this post were sown when Gary Taubes emailed me about a study published in early 2009 in the New England Journal of Medicine (NEJM) that I had seen at the time, briefly skimmed and tossed aside as worthless.  Gary agreed that the study was of little value, but notice that it contained a peculiar statement by the authors, an interesting admission about HDL, the lipophobe’s favorite lipoprotein.  And not only had the authors made this strange admission, but so had another prominent lipophobe who wrote the accompanying editorial.

I pulled the study, read it more thoroughly and still found it mediocre at best.  But I did come across the strange HDL statements that Gary had mentioned. (More about which later.)

As I was shaking my head over the amount of money spent on what was a truly abominable study, the synchronicity occurred.  I got a ding that I had a new email.  It was a notice from the American Heart Association telling me that this august body had deemed the very study I was holding in my hands as one of the ten most important papers published in 2009.  The sheer stupidity of it nearly took my breath away.

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In the early 1980s MD and I were laboring away in anonymity in our clinics in Little Rock, Arkansas.  By that time I had gone through my thin-to fat-to thin again metamorphosis, and I was starting to treat patients for obesity.  My own transformation had been fairly striking, a fact not lost on many of my overweight patients, a number of whom were seeking my professional advice on treating their own weight problems.  I was still doing a fair amount of general primary care medicine, but more and more of my time was being diverted to helping people lose weight.

When I, myself, had gotten fat, I had tried a few diets that were then being extolled (including the Pritikin diet) and had experienced pretty much the same thing most people did with these diets:  I lost a few pounds, drifted from the diet, and regained the lost weight plus a little.  I then started thinking seriously about obesity as a medical problem, and in an effort to learn all I could about it, I turned to the medical textbooks on my shelves.  Unfortunately, none of them contained any information I found particularly enlightening.  The texts went into great detail about the risks associated with obesity and the many diseases that it either caused or made worse, but, other than recommending caloric restriction, none really discussed the treatment.  None really discussed (at least not to my satisfaction) what happens metabolically that makes people store excess fat.

I next turned to physiology texts, which didn’t help a lot, either.  I then grabbed my old medical school biochemistry textbook (I hadn’t been out of med school all that long at the time, so it was fairly current) and struck gold.  I started tracing out all the pathways for fat storage and noticed that in virtually every one insulin turned up somewhere.  Then I started reading about all the pathways involving insulin and realized that excess insulin had to be the agent driving the storage of excess fat.  I then went back to the physiology texts, reread them in light of my new found knowledge, and discovered that they reinforced what I had learned from the biochemistry text. I just hadn’t realized it, until I had made the insulin connection. (I drew out all the different pathways insulin worked through on piece of paper that we’ve saved, but I can’t lay my hands on it right now.  If I find it, I’ll post it.)

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